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cgp46381  (Tocris)


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    Tocris cgp46381
    Cgp46381, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cgp46381/product/Tocris
    Average 94 stars, based on 28 article reviews
    cgp46381 - by Bioz Stars, 2026-02
    94/100 stars

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    Figure 4. Effects of GABBR2 inhibitor or knockdown on the viability of bladder cancer cells. The MTT assay in UMUC3 (A), 5637-AR (B), or 647V-AR (C) cultured in the absence or presence of various doses of <t>CGP46381</t> or UMUC3-control-shRNA vs. UMUC3-GABBR2-shRNA (D) for 48 h. Cell viability representing the mean (+SD) from a total of six determinants is presented relative to that of mock treatment or control subline.
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    ECM depletion affects electrophysiological properties in single neurons and strengthens inhibitory synapses. Spiking frequency, action potential threshold, resting membrane potential, and membrane capacitance were evaluated in the fast-spiking inhibitory interneurons ( a ) and the excitatory neurons ( b ). The results were obtained from 5 independent experiments. c Patch clamp recordings in presence of sodium channel blocker (TTX) and glutamate receptor <t>antagonists</t> (DNQX and D-AP5) reveal miniature inhibitory postsynaptic currents (mIPSCs). Representative current tracks exemplify mIPSCs detected in control and ECM depleted cultures. Quantifications of mIPSC amplitude and frequency indicate that ECM depletion increased the total inhibitory input to single neurons ( n ≥ 19 neurons per condition, results obtained from 5 independent experiments). Data are medians (lines inside boxes)/ means (filled squares inside boxes) ± IQR (boxes) with 10/ 90% ranks as whiskers. Open diamonds are data points. The asterisks indicate significant differences with control, based on Kruskal–Wallis tests (* p < 0.05, *** p < 0.001)
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    ECM depletion affects electrophysiological properties in single neurons and strengthens inhibitory synapses. Spiking frequency, action potential threshold, resting membrane potential, and membrane capacitance were evaluated in the fast-spiking inhibitory interneurons ( a ) and the excitatory neurons ( b ). The results were obtained from 5 independent experiments. c Patch clamp recordings in presence of sodium channel blocker (TTX) and glutamate receptor <t>antagonists</t> (DNQX and D-AP5) reveal miniature inhibitory postsynaptic currents (mIPSCs). Representative current tracks exemplify mIPSCs detected in control and ECM depleted cultures. Quantifications of mIPSC amplitude and frequency indicate that ECM depletion increased the total inhibitory input to single neurons ( n ≥ 19 neurons per condition, results obtained from 5 independent experiments). Data are medians (lines inside boxes)/ means (filled squares inside boxes) ± IQR (boxes) with 10/ 90% ranks as whiskers. Open diamonds are data points. The asterisks indicate significant differences with control, based on Kruskal–Wallis tests (* p < 0.05, *** p < 0.001)
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    ECM depletion affects electrophysiological properties in single neurons and strengthens inhibitory synapses. Spiking frequency, action potential threshold, resting membrane potential, and membrane capacitance were evaluated in the fast-spiking inhibitory interneurons ( a ) and the excitatory neurons ( b ). The results were obtained from 5 independent experiments. c Patch clamp recordings in presence of sodium channel blocker (TTX) and glutamate receptor <t>antagonists</t> (DNQX and D-AP5) reveal miniature inhibitory postsynaptic currents (mIPSCs). Representative current tracks exemplify mIPSCs detected in control and ECM depleted cultures. Quantifications of mIPSC amplitude and frequency indicate that ECM depletion increased the total inhibitory input to single neurons ( n ≥ 19 neurons per condition, results obtained from 5 independent experiments). Data are medians (lines inside boxes)/ means (filled squares inside boxes) ± IQR (boxes) with 10/ 90% ranks as whiskers. Open diamonds are data points. The asterisks indicate significant differences with control, based on Kruskal–Wallis tests (* p < 0.05, *** p < 0.001)
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    Tocris antagonist cgp46381
    ECM depletion affects electrophysiological properties in single neurons and strengthens inhibitory synapses. Spiking frequency, action potential threshold, resting membrane potential, and membrane capacitance were evaluated in the fast-spiking inhibitory interneurons ( a ) and the excitatory neurons ( b ). The results were obtained from 5 independent experiments. c Patch clamp recordings in presence of sodium channel blocker (TTX) and glutamate receptor <t>antagonists</t> (DNQX and D-AP5) reveal miniature inhibitory postsynaptic currents (mIPSCs). Representative current tracks exemplify mIPSCs detected in control and ECM depleted cultures. Quantifications of mIPSC amplitude and frequency indicate that ECM depletion increased the total inhibitory input to single neurons ( n ≥ 19 neurons per condition, results obtained from 5 independent experiments). Data are medians (lines inside boxes)/ means (filled squares inside boxes) ± IQR (boxes) with 10/ 90% ranks as whiskers. Open diamonds are data points. The asterisks indicate significant differences with control, based on Kruskal–Wallis tests (* p < 0.05, *** p < 0.001)
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    Figure 4. Effects of GABBR2 inhibitor or knockdown on the viability of bladder cancer cells. The MTT assay in UMUC3 (A), 5637-AR (B), or 647V-AR (C) cultured in the absence or presence of various doses of CGP46381 or UMUC3-control-shRNA vs. UMUC3-GABBR2-shRNA (D) for 48 h. Cell viability representing the mean (+SD) from a total of six determinants is presented relative to that of mock treatment or control subline.

    Journal: International journal of molecular sciences

    Article Title: GABBR2 as a Downstream Effector of the Androgen Receptor Induces Cisplatin Resistance in Bladder Cancer.

    doi: 10.3390/ijms241813733

    Figure Lengend Snippet: Figure 4. Effects of GABBR2 inhibitor or knockdown on the viability of bladder cancer cells. The MTT assay in UMUC3 (A), 5637-AR (B), or 647V-AR (C) cultured in the absence or presence of various doses of CGP46381 or UMUC3-control-shRNA vs. UMUC3-GABBR2-shRNA (D) for 48 h. Cell viability representing the mean (+SD) from a total of six determinants is presented relative to that of mock treatment or control subline.

    Article Snippet: DHT and HF, CGP46381, and CDDP were obtained from Sigma-Aldrich (St. Louis, MO, USA), Thermo Fisher (Waltham, MA, USA), and Santa Cruz Biotechnology (Dallas, TX, USA), respectively.

    Techniques: Knockdown, MTT Assay, Cell Culture, Control, shRNA

    Figure 5. Effects of GABBR2 inhibitor or knockdown on the migration of bladder cancer cells. The wound-healing assay in UMUC3 (A), 5637-AR (B), or 647V-AR (C) without or with CGP46381 (5 µM) or UMUC3-control-shRNA vs. UMUC3-GABBR2-shRNA (D) cultured for 24 h after scratching. Cell migration determined by the rate of cells filling the wound area is presented relative to that of mock treatment or control subline. Each value represents the mean (+SD) from a total of six determinants.

    Journal: International journal of molecular sciences

    Article Title: GABBR2 as a Downstream Effector of the Androgen Receptor Induces Cisplatin Resistance in Bladder Cancer.

    doi: 10.3390/ijms241813733

    Figure Lengend Snippet: Figure 5. Effects of GABBR2 inhibitor or knockdown on the migration of bladder cancer cells. The wound-healing assay in UMUC3 (A), 5637-AR (B), or 647V-AR (C) without or with CGP46381 (5 µM) or UMUC3-control-shRNA vs. UMUC3-GABBR2-shRNA (D) cultured for 24 h after scratching. Cell migration determined by the rate of cells filling the wound area is presented relative to that of mock treatment or control subline. Each value represents the mean (+SD) from a total of six determinants.

    Article Snippet: DHT and HF, CGP46381, and CDDP were obtained from Sigma-Aldrich (St. Louis, MO, USA), Thermo Fisher (Waltham, MA, USA), and Santa Cruz Biotechnology (Dallas, TX, USA), respectively.

    Techniques: Knockdown, Migration, Wound Healing Assay, Control, shRNA, Cell Culture

    Figure 7. Effects of GABBR2 inhibitor on CDDP cytotoxicity in bladder cancer cells. The MTT assay in UMUC3 (A), 5637-AR (B), or 647V-AR (C) without or with CGP46381 (5 µM) or UMUC3-control- shRNA or UMUC3-GABBR2-shRNA (D) cultured for 48 h in the absence or presence of CDDP (5 µM). Cell viability representing the mean (+SD) from a total of six determinants is presented relative to that of mock or CGP46381 treatment (without vs. with CDDP) in each subline. * p < 0.05 [vs. CDDP(+)/CGP46381(−) cells].

    Journal: International journal of molecular sciences

    Article Title: GABBR2 as a Downstream Effector of the Androgen Receptor Induces Cisplatin Resistance in Bladder Cancer.

    doi: 10.3390/ijms241813733

    Figure Lengend Snippet: Figure 7. Effects of GABBR2 inhibitor on CDDP cytotoxicity in bladder cancer cells. The MTT assay in UMUC3 (A), 5637-AR (B), or 647V-AR (C) without or with CGP46381 (5 µM) or UMUC3-control- shRNA or UMUC3-GABBR2-shRNA (D) cultured for 48 h in the absence or presence of CDDP (5 µM). Cell viability representing the mean (+SD) from a total of six determinants is presented relative to that of mock or CGP46381 treatment (without vs. with CDDP) in each subline. * p < 0.05 [vs. CDDP(+)/CGP46381(−) cells].

    Article Snippet: DHT and HF, CGP46381, and CDDP were obtained from Sigma-Aldrich (St. Louis, MO, USA), Thermo Fisher (Waltham, MA, USA), and Santa Cruz Biotechnology (Dallas, TX, USA), respectively.

    Techniques: MTT Assay, Control, shRNA, Cell Culture

    ECM depletion affects electrophysiological properties in single neurons and strengthens inhibitory synapses. Spiking frequency, action potential threshold, resting membrane potential, and membrane capacitance were evaluated in the fast-spiking inhibitory interneurons ( a ) and the excitatory neurons ( b ). The results were obtained from 5 independent experiments. c Patch clamp recordings in presence of sodium channel blocker (TTX) and glutamate receptor antagonists (DNQX and D-AP5) reveal miniature inhibitory postsynaptic currents (mIPSCs). Representative current tracks exemplify mIPSCs detected in control and ECM depleted cultures. Quantifications of mIPSC amplitude and frequency indicate that ECM depletion increased the total inhibitory input to single neurons ( n ≥ 19 neurons per condition, results obtained from 5 independent experiments). Data are medians (lines inside boxes)/ means (filled squares inside boxes) ± IQR (boxes) with 10/ 90% ranks as whiskers. Open diamonds are data points. The asterisks indicate significant differences with control, based on Kruskal–Wallis tests (* p < 0.05, *** p < 0.001)

    Journal: Cellular and Molecular Life Sciences

    Article Title: Inhibitory control in neuronal networks relies on the extracellular matrix integrity

    doi: 10.1007/s00018-021-03861-3

    Figure Lengend Snippet: ECM depletion affects electrophysiological properties in single neurons and strengthens inhibitory synapses. Spiking frequency, action potential threshold, resting membrane potential, and membrane capacitance were evaluated in the fast-spiking inhibitory interneurons ( a ) and the excitatory neurons ( b ). The results were obtained from 5 independent experiments. c Patch clamp recordings in presence of sodium channel blocker (TTX) and glutamate receptor antagonists (DNQX and D-AP5) reveal miniature inhibitory postsynaptic currents (mIPSCs). Representative current tracks exemplify mIPSCs detected in control and ECM depleted cultures. Quantifications of mIPSC amplitude and frequency indicate that ECM depletion increased the total inhibitory input to single neurons ( n ≥ 19 neurons per condition, results obtained from 5 independent experiments). Data are medians (lines inside boxes)/ means (filled squares inside boxes) ± IQR (boxes) with 10/ 90% ranks as whiskers. Open diamonds are data points. The asterisks indicate significant differences with control, based on Kruskal–Wallis tests (* p < 0.05, *** p < 0.001)

    Article Snippet: To study the impact of ECM depletion on GABAergic neurotransmission, GABA A (6 μM bicuculline metiodide, Tocris) or GABA B (100 μM CGP46381, Tocris) receptor antagonists were applied.

    Techniques: Membrane, Patch Clamp, Control